Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines
Abstract
Our purpose is to examine the role of the NF1 gene product, neurofibromin, in modulating the migratory and invasive properties of neural crest cells (NCC) and neural crest-derived sarcoma cells. As a negative regulator of Ras signaling, neurofibromin may influence the responses of NC-derived cells to growth factors and extracellular matrix (ECM) molecules that affect motility. We use embryonic NCC and NC-derived sarcoma lines isolated from cisNf1;p53 mice to compare integrin ECM receptor expression patterns, ECM adhesion preferences, migration on ECM substrata, invasion through ECM barriers, and dispersal along NCC pathways in vivo for wild-type and neurofibromin-deficient cells. In the past year, we have completed studies on the invasiveness of branchial arch mesenchymal cells and trigeminal neural crest cells isolated from Nf-/-, +/-, and +/+ mouse embryos. Consistent with published results for neurofibromin deficient astrocytes, mast cells, and Schwann cells, our data indicate that Nf1 mutant cranial neural crest cell populations are more invasive through laminin and fibronectin matrices.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2003
- Accession Number
- ADA422403
Entities
People
- Kristine S. Vogel
Organizations
- University of Texas Health Science Center at San Antonio